Congenital adrenal hyperplasia (salt losers): Limited data available: Oral: Maintenance therapy: 0.05 to 0.2 mg daily in 1 or 2 divided doses; in newborns, doses as high as 0.4 mg/day may be necessary; use in combination with glucocorticoid therapy (eg, hydrocortisone) and sodium replacement therapy (Endocrine Society [Speiser 2018]; Sperling 2014).
Note: Dosing should be individualized to lowest effective dose.
Adrenal insufficiency, autoimmune (primary adrenal insufficiency, aldosterone deficiency component Addison disease); replacement therapy: Limited data available: Infants, Children, and Adolescents: Oral: 0.05 to 0.2 mg daily (Betterle 2002; Endocrine Society [Bornstein 2016]; Kliegman 2020).
Congenital adrenal hyperplasia (salt losers) (eg, 21-hydroxylase deficiency): Limited data available: Note: Use in combination with glucocorticoid therapy (eg, hydrocortisone); concurrent sodium replacement therapy may be required, particularly in young infants.
Maintenance therapy:
Infants, Children, and Adolescents (actively growing): Oral: Usual range: 0.05 to 0.2 mg daily in 1 or 2 divided doses; doses as high as 0.3 mg/day may be necessary (AAP 2000; Endocrine Society [Speiser 2018]).
Adolescents (fully grown): Oral: 0.05 to 0.2 mg once daily (Endocrine Society [Speiser 2018]).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer's labeling; use with caution.
There are no dosage adjustments provided in the manufacturer's labeling.
(For additional information see "Fludrocortisone: Drug information")
Note: Due to risk of hypokalemia, periodically monitor serum potassium during therapy; ensure adequate dietary potassium intake as appropriate (EFNS [Lahrmann 2006]; manufacturer's labeling).
Adrenal insufficiency, primary (Addison disease): Oral: Initial: 0.05 to 0.1 mg once daily in the morning (in combination with glucocorticoid therapy). Usual maintenance dose: 0.05 to 0.2 mg once daily. If hypertension develops, dose reduction is suggested; an antihypertensive may be necessary if hypertension remains uncontrolled (ES [Bornstein 2016]).
Congenital adrenal hyperplasia, classic (salt-losing adrenogenital syndrome): Oral: 0.05 to 0.2 mg/day in 1 or 2 divided doses (in combination with glucocorticoid therapy) (ES [Speiser 2018]).
Orthostatic hypotension (off-label use):
Note: For use in conjunction with nonpharmacologic measures (eg, high-salt diet, adequate fluid intake, head-up tilt sleeping). Use with caution or avoid in patients with heart failure or low serum albumin (EFNS [Lahrmann 2006]; ESC [Brignole 2018]; Palma 2020).
Oral: Initial: 0.05 to 0.1 mg once daily (Palma 2020; Schoffer 2007; Ten Harkel 1992). May adjust dose (eg, in 0.05 to 0.1 mg/day increments) at weekly intervals if needed based on response; usual dose range: 0.05 to 0.2 mg/day administered in 1 or 2 divided daily doses (Campbell 1976; EFNS [Lahrmann 2006]; Palma 2020; Schoffer 2007; Ten Harkel 1992; van Lieshout 2000). Doses >0.2 mg/day have been associated with an increased risk of adverse effects without added benefit (EFNS [Lahrmann 2006]; Palma 2020).
Postural orthostatic tachycardia syndrome (off-label use):
Oral: Initial: 0.05 to 0.1 mg once daily. May increase slowly based on response and tolerability up to 0.1 to 0.2 mg/day (Bryarly 2019; Cheshire 2022; Mar 2020).
Septic shock (off-label use): Note: Consider corticosteroids in patients with ongoing vasopressor requirements (SCCM/ESICM [Annane 2017]; SSC [Evans 2021]). Oral: 0.05 mg once daily (via nasogastric tube) for 7 days (in combination with IV hydrocortisone) (Annane 2002; Annane 2018).
Dosage adjustment for concomitant therapy: Significant drug interactions exist, requiring dose/frequency adjustment or avoidance. Consult drug interactions database for more information.
There are no dosage adjustments provided in the manufacturer's labeling; use with caution.
There are no dosage adjustments provided in the manufacturer's labeling; use with caution.
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral, as acetate:
Generic: 0.1 mg
Yes
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Tablet, Oral, as acetate:
Florinef: 0.1 mg
Oral: May administer without regard to food; if GI upset, may take with food. Tablets may be crushed and mixed with about 1 teaspoon of water or soft food such as applesauce, chocolate syrup, jelly, or yogurt.
Oral: Administer without regard to food; if GI upset, may take with food. For septic shock (off-label use), administer via nasogastric tube (Annane 2002; Annane 2018)
Store at 15°C to 30°C (59°F to 86°F); avoid excessive heat. The Canadian labeling recommends to store at 2°C to 8°C (36°F to 46°F).
Partial replacement therapy for primary and secondary adrenocortical insufficiency in Addison disease; treatment of salt-losing adrenogenital syndrome (or congenital adrenal hyperplasia) (All indications: FDA approved in adults).
Florinef may be confused with Fioricet, Fiorinal, Floranex, Florastor
Fludrocortisone is associated with hypertension (most commonly supine systolic) and heart failure with reduced ejection fraction (HFrEF) (Ref). When using fludrocortisone to treat orthostatic hypotension (OH), it is important to consider comorbid conditions, as fludrocortisone patients have an increased risk of heart failure and all cause hospitalization (Ref). Supine hypertension was more common with autonomic failure (Ref). In a study of older adults with OH, the incidence of hypertension and acute HFrEF was estimated at 6% and 11%, respectively (Ref). Development of HFrEF after initiation of fludrocortisone for treatment of adrenal insufficiency, although rare, is documented in 3 cases across all age groups (Ref). Children receiving fludrocortisone for congenital adrenal hyperplasia (CAH) have a higher incidence of hypertension (55%) compared to children not receiving fludrocortisone (31%) (Ref).
Mechanism: Transient increase in plasma volume due to potent mineralocorticoid activity promoting sodium retention, thereby expanding plasma volume and increasing cardiac afterload (Ref). Sustained changes in blood pressure are from heightened sensitivity of alpha-adrenoreceptors and enhanced release of norepinephrine and angiotensin II (Ref). Long-term use may promote cardiac fibrosis, oxidative stress, and endothelial dysfunction that could affect cardiac remolding (Ref).
Onset: Varies; heart failure has been reported within 2 to 3 weeks after therapy initiation (Ref) and following long-term use (Ref). In a study of older adults with OH, the mean time to development of hypertension and heart failure was 5 months and 7 months, respectively (Ref).
Risk factors:
• Long-term treatment (independent of dose) in older adults with OH (Ref)
• History of HFrEF (Ref)
• History of Addison disease (Ref)
• Dose in children <8 years of age with CAH (Ref)
Fludrocortisone is associated with hypokalemia and hypomagnesemia (Ref). In 2 studies of adults with orthostatic hypotension, the incidence of hypokalemia and hypomagnesemia was estimated at 24% to 50% and ~5%, respectively (Ref). These electrolyte disturbances have the potential to further exacerbate underlying conditions (eg, arrhythmias), especially in those with heart failure with reduced ejection fraction (Ref). Hypomagnesemia was not reported in children receiving fludrocortisone for the treatment of primary adrenal insufficiency for an average of 6.5 years (Ref).
Mechanism: Effect on the distal tubule in the kidney elicit sodium ion and water transport into the plasma, thereby increasing potassium and hydrogen ions into the urine (Ref).
Onset: Varies; duration of therapy prior to development of hypokalemia ranges from within 1 week to several months (Ref). In a study with older adults with orthostatic hypotension, the mean onset was 8 months (range: 2 to 21 months) (Ref).
Risk factors:
• Concurrent amphotericin B, diuretics, or digoxin
The following adverse drug reactions and incidences are derived from product labeling unless otherwise specified.
Frequency not defined:
Cardiovascular: Cardiomegaly, edema, heart failure (Grijalva 2017), hypertension (Bonfig 2015; Grijalva 2017)
Dermatologic: Allergic skin rash, atrophic striae, diaphoresis, ecchymoses, facial erythema, hyperpigmentation (skin and nails), maculopapular rash, skin atrophy, subcutaneous atrophy, urticaria
Endocrine & metabolic: Cushing syndrome, growth retardation, hirsutism, HPA-axis suppression, hyperglycemia, hypokalemia (Grijalva 2017), hypokalemic alkalosis, menstrual disease, negative nitrogen balance, prediabetes
Gastrointestinal: Abdominal distention, esophageal ulcer, pancreatitis, peptic ulcer
Genitourinary: Glycosuria
Hematologic & oncologic: Bruise, petechia, purpuric disease
Local: Local acneiform eruptions
Nervous system: Amyotrophy, headache, intracranial hypertension (idiopathic), mental status changes (severe), myasthenia, seizure, vertigo
Neuromuscular & skeletal: Aseptic necrosis of femoral head, aseptic necrosis of humeral head, bone fracture (including pathological fracture and vertebral compression fracture), osteoporosis, steroid myopathy
Ophthalmic: Exophthalmos, glaucoma, subcapsular posterior cataract
Miscellaneous: Wound healing impairment
Postmarketing:
Endocrine & metabolic: Hypomagnesemia (Grijalva 2017)
Respiratory: Pulmonary edema (Misra 2018)
Hypersensitivity to fludrocortisone or any component of the formulation; systemic fungal infections
Documentation of allergenic cross-reactivity for corticosteroids is limited. However, because of similarities in chemical structure and/or pharmacologic actions, the possibility of cross-sensitivity cannot be ruled out with certainty.
Concerns related to adverse effects:
• Adrenal suppression: May cause hypercortisolism or suppression of hypothalamic-pituitary-adrenal (HPA) axis, particularly in younger children or in patients receiving high doses for prolonged periods. HPA axis suppression may lead to adrenal crisis. Withdrawal and discontinuation of a corticosteroid should be done slowly and carefully.
• Anaphylactoid reactions: Rare cases of anaphylactoid reactions have been observed in patients receiving corticosteroids.
• Immunosuppression: Prolonged use may increase risk of infection, mask acute infection (including fungal infections), prolong or exacerbate viral infections, or limit response to killed or inactivated vaccines. Exposure to chickenpox or measles should be avoided. Corticosteroids should not be used for cerebral malaria or viral hepatitis. Close observation is required in patients with latent tuberculosis (TB) and/or TB reactivity. Restrict use in active TB (only fulminating or disseminated TB in conjunction with antituberculosis treatment). Amebiasis should be ruled out in any patient with recent travel to tropic climates or unexplained diarrhea prior to initiation of corticosteroids. Use with extreme caution in patients with Strongyloides infections; hyperinfection, dissemination and fatalities have occurred.
• Kaposi sarcoma: Prolonged treatment with corticosteroids has been associated with the development of Kaposi sarcoma (case reports); if noted, discontinuation of therapy should be considered (Goedert 2002).
• Myopathy: Acute myopathy has been reported with high-dose corticosteroids, usually in patients with neuromuscular transmission disorders; may involve ocular and/or respiratory muscles; monitor creatine kinase; recovery may be delayed.
• Psychiatric disturbances: Corticosteroid use may cause psychiatric disturbances, including euphoria, insomnia, mood swings, personality changes, severe depression to psychotic manifestation. Preexisting psychiatric conditions may be exacerbated by corticosteroid use.
Disease-related concerns:
• Cardiovascular disease: Use with caution in patients with HF and/or hypertension; use may be associated with fluid retention, electrolyte disturbances, and hypertension. Use with caution following acute MI; corticosteroids have been associated with myocardial rupture.
• Diabetes: Use corticosteroids with caution in patients with diabetes mellitus; may alter glucose production/regulation leading to hyperglycemia.
• Gastrointestinal disease: Use with caution in patients with GI diseases (diverticulitis, fresh intestinal anastomoses, active or latent peptic ulcer, ulcerative colitis, abscess or other pyogenic infection) due to perforation risk.
• Hepatic impairment: Use with caution in patients with hepatic impairment, including cirrhosis; long-term use has been associated with fluid retention.
• Kidney impairment: Use with caution in patients with kidney impairment; fluid retention may occur.
• Myasthenia gravis: Use may cause transient worsening of myasthenia gravis (MG) (eg, within first 2 weeks of treatment); monitor for worsening MG (AAN [Narayanaswami 2021]).
• Ocular disease: Use with caution in patients with cataracts and/or glaucoma; increased intraocular pressure, open-angle glaucoma, and cataracts have occurred with prolonged use. Use with caution in patients with a history of ocular herpes simplex; corneal perforation has occurred; do not use in active ocular herpes simplex. Consider routine eye exams in chronic users.
• Osteoporosis: Use with caution in patients with osteoporosis; high doses and/or long-term use of corticosteroids have been associated with increased bone loss and osteoporotic fractures.
• Seizure disorders: Use corticosteroids with caution in patients with a history of seizure disorder; seizures have been reported with adrenal crisis.
• Systemic sclerosis: Use with caution in patients with systemic sclerosis; an increase in scleroderma renal crisis incidence has been observed with corticosteroid use. Monitor BP and kidney function in patients with systemic sclerosis treated with corticosteroids (EULAR [Kowal-Bielecka 2017]).
• Thyroid disease: Changes in thyroid status may necessitate dosage adjustments; metabolic clearance of corticosteroids increases in hyperthyroid patients and decreases in hypothyroid ones.
Special populations:
• Older adults: Because of the risk of adverse effects, use with caution in older adults; use with the smallest possible effective dose for the shortest duration.
• Pediatric: May affect growth velocity; growth and development should be routinely monitored in pediatric patients.
Other warnings/precautions:
• Discontinuation of therapy: Withdraw therapy with gradual tapering of dose.
• Stress: Patients may require higher doses when subject to stress (ie, trauma, surgery, severe illness).
May cause osteoporosis (at any age) or inhibition of bone growth in pediatric patients. Use with caution in patients with osteoporosis. In a population-based study of children, risk of fracture was shown to be increased with >4 courses of corticosteroids; underlying clinical condition may also impact bone health and osteoporotic effect of corticosteroids (Leonard 2007). Hypertrophic cardiomyopathy has been reported in premature neonates.
Substrate of CYP3A4 (minor); Note: Assignment of Major/Minor substrate status based on clinically relevant drug interaction potential
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program by clicking on the “Launch drug interactions program” link above.
Note: Interacting drugs may not be individually listed below if they are part of a group interaction (eg, individual drugs within “CYP3A4 Inducers [Strong]” are NOT listed). For a complete list of drug interactions by individual drug name and detailed management recommendations, use the Lexicomp drug interactions program
Abrocitinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Abrocitinib. Management: The use of abrocitinib in combination with other immunosuppressants is not recommended. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks are considered immunosuppressive. Risk D: Consider therapy modification
Acetylcholinesterase Inhibitors: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Acetylcholinesterase Inhibitors. Increased muscular weakness may occur. Risk C: Monitor therapy
Aldesleukin: Corticosteroids may diminish the antineoplastic effect of Aldesleukin. Risk X: Avoid combination
Amphotericin B: Corticosteroids (Systemic) may enhance the hypokalemic effect of Amphotericin B. Risk C: Monitor therapy
Androgens: Corticosteroids (Systemic) may enhance the fluid-retaining effect of Androgens. Risk C: Monitor therapy
Antacids: May decrease the bioavailability of Corticosteroids (Oral). Management: Consider separating doses by 2 or more hours. Budesonide enteric coated tablets could dissolve prematurely if given with drugs that lower gastric acid, with unknown impact on budesonide therapeutic effects. Risk D: Consider therapy modification
Antidiabetic Agents: Hyperglycemia-Associated Agents may diminish the therapeutic effect of Antidiabetic Agents. Risk C: Monitor therapy
Baricitinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Baricitinib. Management: The use of baricitinib in combination with potent immunosuppressants is not recommended. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks are considered immunosuppressive. Risk D: Consider therapy modification
BCG Products: Corticosteroids (Systemic) may enhance the adverse/toxic effect of BCG Products. Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of BCG Products. Risk X: Avoid combination
Bile Acid Sequestrants: May decrease the absorption of Corticosteroids (Oral). Risk C: Monitor therapy
Brincidofovir: Corticosteroids (Systemic) may diminish the therapeutic effect of Brincidofovir. Risk C: Monitor therapy
Calcitriol (Systemic): Corticosteroids (Systemic) may diminish the therapeutic effect of Calcitriol (Systemic). Risk C: Monitor therapy
CAR-T Cell Immunotherapy: Corticosteroids (Systemic) may enhance the adverse/toxic effect of CAR-T Cell Immunotherapy. Specifically, the severity and duration of neurologic toxicities may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of CAR-T Cell Immunotherapy. Management: Avoid use of corticosteroids as premedication before treatment with CAR-T cell immunotherapy agents. Corticosteroids are indicated and may be required for treatment of toxicities such as cytokine release syndrome or neurologic toxicity. Risk D: Consider therapy modification
Cladribine: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Cladribine. Risk X: Avoid combination
Coccidioides immitis Skin Test: Corticosteroids (Systemic) may diminish the diagnostic effect of Coccidioides immitis Skin Test. Management: Consider discontinuing systemic corticosteroids (dosed at 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks) several weeks prior to coccidioides immitis skin antigen testing. Risk D: Consider therapy modification
Corticorelin: Corticosteroids (Systemic) may diminish the therapeutic effect of Corticorelin. Specifically, the plasma ACTH response to corticorelin may be blunted by recent or current corticosteroid therapy. Risk C: Monitor therapy
Cosyntropin: Corticosteroids (Systemic) may diminish the diagnostic effect of Cosyntropin. Risk C: Monitor therapy
COVID-19 Vaccine (Adenovirus Vector): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (Adenovirus Vector). Management: Administer a 2nd dose using an mRNA COVID-19 vaccine (at least 4 weeks after the primary vaccine dose) and a bivalent booster dose (at least 2 months after the additional mRNA dose or any other boosters) Risk D: Consider therapy modification
COVID-19 Vaccine (Inactivated Virus): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (Inactivated Virus). Risk C: Monitor therapy
COVID-19 Vaccine (mRNA): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (mRNA). Management: Give a 3-dose primary series for all patients aged 6 months and older taking immunosuppressive medications or therapies. Booster doses are recommended for certain age groups. See CDC guidance for details. Risk D: Consider therapy modification
COVID-19 Vaccine (Subunit): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (Subunit). Risk C: Monitor therapy
COVID-19 Vaccine (Virus-like Particles): Corticosteroids (Systemic) may diminish the therapeutic effect of COVID-19 Vaccine (Virus-like Particles). Risk C: Monitor therapy
Deferasirox: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Deferasirox. Specifically, the risk for GI ulceration/irritation or GI bleeding may be increased. Risk C: Monitor therapy
Dengue Tetravalent Vaccine (Live): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Dengue Tetravalent Vaccine (Live). Specifically, the risk of vaccine associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Dengue Tetravalent Vaccine (Live). Risk X: Avoid combination
Denosumab: May enhance the immunosuppressive effect of Corticosteroids (Systemic). Management: Consider the risk of serious infections versus the potential benefits of coadministration of denosumab and systemic corticosteroids. If combined, monitor patients for signs/symptoms of serious infections. Risk D: Consider therapy modification
Desirudin: Corticosteroids (Systemic) may enhance the anticoagulant effect of Desirudin. More specifically, corticosteroids may increase hemorrhagic risk during desirudin treatment. Management: Discontinue treatment with systemic corticosteroids prior to desirudin initiation. If concomitant use cannot be avoided, monitor patients receiving these combinations closely for clinical and laboratory evidence of excessive anticoagulation. Risk D: Consider therapy modification
Desmopressin: Corticosteroids (Systemic) may enhance the hyponatremic effect of Desmopressin. Risk X: Avoid combination
Deucravacitinib: May enhance the immunosuppressive effect of Corticosteroids (Systemic). Management: The use of deucravacitinib in combination with potent immunosuppressants is not recommended. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks are considered immunosuppressive. Risk D: Consider therapy modification
Estrogen Derivatives: May increase the serum concentration of Corticosteroids (Systemic). Risk C: Monitor therapy
Filgotinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Filgotinib. Management: Coadministration of filgotinib with systemic corticosteroids at doses equivalent to greater than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks is not recommended. Risk D: Consider therapy modification
Gallium Ga 68 Dotatate: Corticosteroids (Systemic) may diminish the diagnostic effect of Gallium Ga 68 Dotatate. Risk C: Monitor therapy
Growth Hormone Analogs: Corticosteroids (Systemic) may diminish the therapeutic effect of Growth Hormone Analogs. Growth Hormone Analogs may decrease serum concentrations of the active metabolite(s) of Corticosteroids (Systemic). Risk C: Monitor therapy
Hyaluronidase: Corticosteroids (Systemic) may diminish the therapeutic effect of Hyaluronidase. Management: Patients receiving corticosteroids (particularly at larger doses) may not experience the desired clinical response to standard doses of hyaluronidase. Larger doses of hyaluronidase may be required. Risk D: Consider therapy modification
Immune Checkpoint Inhibitors: Corticosteroids (Systemic) may diminish the therapeutic effect of Immune Checkpoint Inhibitors. Management: Carefully consider the need for corticosteroids, at doses of a prednisone-equivalent of 10 mg or more per day, during the initiation of immune checkpoint inhibitor therapy. Use of corticosteroids to treat immune related adverse events is still recommended Risk D: Consider therapy modification
Indium 111 Capromab Pendetide: Corticosteroids (Systemic) may diminish the diagnostic effect of Indium 111 Capromab Pendetide. Risk X: Avoid combination
Inebilizumab: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Inebilizumab. Risk C: Monitor therapy
Influenza Virus Vaccines: Corticosteroids (Systemic) may diminish the therapeutic effect of Influenza Virus Vaccines. Management: Administer influenza vaccines at least 2 weeks prior to initiation of systemic corticosteroids at immunosuppressive doses. Influenza vaccines administered less than 14 days prior to or during such therapy should be repeated 3 months after therapy. Risk D: Consider therapy modification
Isoniazid: Corticosteroids (Systemic) may decrease the serum concentration of Isoniazid. Risk C: Monitor therapy
Leflunomide: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Leflunomide. Management: Increase the frequency of chronic monitoring of platelet, white blood cell count, and hemoglobin or hematocrit to monthly, instead of every 6 to 8 weeks, if leflunomide is coadministered with immunosuppressive agents, such as systemic corticosteroids. Risk D: Consider therapy modification
Licorice: May increase the serum concentration of Corticosteroids (Systemic). Risk C: Monitor therapy
Loop Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Loop Diuretics. Risk C: Monitor therapy
Lutetium Lu 177 Dotatate: Corticosteroids (Systemic) may diminish the therapeutic effect of Lutetium Lu 177 Dotatate. Management: Avoid repeated use of high-doses of corticosteroids during treatment with lutetium Lu 177 dotatate. Use of corticosteroids is still permitted for the treatment of neuroendocrine hormonal crisis. The effects of lower corticosteroid doses is unknown. Risk D: Consider therapy modification
Macimorelin: Corticosteroids (Systemic) may diminish the diagnostic effect of Macimorelin. Risk X: Avoid combination
MetyraPONE: Corticosteroids (Systemic) may diminish the diagnostic effect of MetyraPONE. Management: Consider alternatives to the use of the metyrapone test in patients taking systemic corticosteroids. Risk D: Consider therapy modification
Mifamurtide: Corticosteroids (Systemic) may diminish the therapeutic effect of Mifamurtide. Risk X: Avoid combination
MiFEPRIStone: May diminish the therapeutic effect of Corticosteroids (Systemic). MiFEPRIStone may increase the serum concentration of Corticosteroids (Systemic). Management: Avoid mifepristone in patients who require long-term corticosteroid treatment of serious illnesses or conditions (eg, for immunosuppression following transplantation). Corticosteroid effects may be reduced by mifepristone treatment. Risk X: Avoid combination
Mineralocorticoid (Aldosterone) Receptor Antagonists: Fludrocortisone may diminish the therapeutic effect of Mineralocorticoid (Aldosterone) Receptor Antagonists. Mineralocorticoid (Aldosterone) Receptor Antagonists may diminish the therapeutic effect of Fludrocortisone. Risk C: Monitor therapy
Natalizumab: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Natalizumab. Risk X: Avoid combination
Neuromuscular-Blocking Agents (Nondepolarizing): May enhance the adverse neuromuscular effect of Corticosteroids (Systemic). Increased muscle weakness, possibly progressing to polyneuropathies and myopathies, may occur. Management: If concomitant therapy is required, use the lowest dose for the shortest duration to limit the risk of myopathy or neuropathy. Monitor for new onset or worsening muscle weakness, reduction or loss of deep tendon reflexes, and peripheral sensory decriments Risk D: Consider therapy modification
Nicorandil: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nicorandil. Gastrointestinal perforation has been reported in association with this combination. Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents (COX-2 Selective): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents (COX-2 Selective). Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents (Nonselective): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Nonsteroidal Anti-Inflammatory Agents (Nonselective). Risk C: Monitor therapy
Nonsteroidal Anti-Inflammatory Agents (Topical): May enhance the adverse/toxic effect of Corticosteroids (Systemic). Specifically, the risk of gastrointestinal bleeding, ulceration, and perforation may be increased. Risk C: Monitor therapy
Ocrelizumab: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ocrelizumab. Risk C: Monitor therapy
Ofatumumab: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ofatumumab. Risk C: Monitor therapy
Pidotimod: Corticosteroids (Systemic) may diminish the therapeutic effect of Pidotimod. Risk C: Monitor therapy
Pimecrolimus: May enhance the immunosuppressive effect of Corticosteroids (Systemic). Risk X: Avoid combination
Pneumococcal Vaccines: Corticosteroids (Systemic) may diminish the therapeutic effect of Pneumococcal Vaccines. Risk C: Monitor therapy
Poliovirus Vaccine (Live/Trivalent/Oral): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Poliovirus Vaccine (Live/Trivalent/Oral). Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Poliovirus Vaccine (Live/Trivalent/Oral). Risk X: Avoid combination
Polymethylmethacrylate: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Polymethylmethacrylate. Specifically, the risk for hypersensitivity or implant clearance may be increased. Management: Use caution when considering use of bovine collagen-containing implants such as the polymethylmethacrylate-based Bellafill brand implant in patients who are receiving immunosuppressants. Consider use of additional skin tests prior to administration. Risk D: Consider therapy modification
Quinolones: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Quinolones. Specifically, the risk of tendonitis and tendon rupture may be increased. Risk C: Monitor therapy
Rabies Vaccine: Corticosteroids (Systemic) may diminish the therapeutic effect of Rabies Vaccine. Management: Complete rabies vaccination at least 2 weeks before initiation of immunosuppressant therapy if possible. If combined, check for rabies antibody titers, and if vaccination is for post exposure prophylaxis, administer a 5th dose of the vaccine. Risk D: Consider therapy modification
Ritodrine: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Ritodrine. Risk C: Monitor therapy
Rubella- or Varicella-Containing Live Vaccines: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Rubella- or Varicella-Containing Live Vaccines. Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Rubella- or Varicella-Containing Live Vaccines. Risk X: Avoid combination
Ruxolitinib (Topical): Corticosteroids (Systemic) may enhance the immunosuppressive effect of Ruxolitinib (Topical). Risk X: Avoid combination
Salicylates: May enhance the adverse/toxic effect of Corticosteroids (Systemic). These specifically include gastrointestinal ulceration and bleeding. Corticosteroids (Systemic) may decrease the serum concentration of Salicylates. Withdrawal of corticosteroids may result in salicylate toxicity. Risk C: Monitor therapy
Sargramostim: Corticosteroids (Systemic) may enhance the therapeutic effect of Sargramostim. Specifically, corticosteroids may enhance the myeloproliferative effects of sargramostim. Risk C: Monitor therapy
Sipuleucel-T: Corticosteroids (Systemic) may diminish the therapeutic effect of Sipuleucel-T. Management: Consider reducing the dose or discontinuing immunosuppressants, such as systemic corticosteroids, prior to initiating sipuleucel-T therapy. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone given for 2 or more weeks are immunosuppressive. Risk D: Consider therapy modification
Sodium Benzoate: Corticosteroids (Systemic) may diminish the therapeutic effect of Sodium Benzoate. Risk C: Monitor therapy
Sphingosine 1-Phosphate (S1P) Receptor Modulator: May enhance the immunosuppressive effect of Corticosteroids (Systemic). Risk C: Monitor therapy
Succinylcholine: Corticosteroids (Systemic) may enhance the neuromuscular-blocking effect of Succinylcholine. Risk C: Monitor therapy
Tacrolimus (Systemic): Corticosteroids (Systemic) may decrease the serum concentration of Tacrolimus (Systemic). Conversely, when discontinuing corticosteroid therapy, tacrolimus concentrations may increase. Risk C: Monitor therapy
Tacrolimus (Topical): Corticosteroids (Systemic) may enhance the immunosuppressive effect of Tacrolimus (Topical). Risk X: Avoid combination
Talimogene Laherparepvec: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Talimogene Laherparepvec. Specifically, the risk of infection from the live, attenuated herpes simplex virus contained in talimogene laherparepvec may be increased. Risk X: Avoid combination
Tertomotide: Corticosteroids (Systemic) may diminish the therapeutic effect of Tertomotide. Risk X: Avoid combination
Thiazide and Thiazide-Like Diuretics: Corticosteroids (Systemic) may enhance the hypokalemic effect of Thiazide and Thiazide-Like Diuretics. Risk C: Monitor therapy
Tofacitinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Tofacitinib. Management: Coadministration of tofacitinib with potent immunosuppressants is not recommended. Doses equivalent to more than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks are considered immunosuppressive. Risk D: Consider therapy modification
Typhoid Vaccine: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Typhoid Vaccine. Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Typhoid Vaccine. Risk X: Avoid combination
Upadacitinib: Corticosteroids (Systemic) may enhance the immunosuppressive effect of Upadacitinib. Management: Coadministration of upadacitinib with systemic corticosteroids at doses equivalent to greater than 2 mg/kg or 20 mg/day of prednisone (for persons over 10 kg) administered for 2 or more weeks is not recommended. Risk D: Consider therapy modification
Urea Cycle Disorder Agents: Corticosteroids (Systemic) may diminish the therapeutic effect of Urea Cycle Disorder Agents. More specifically, Corticosteroids (Systemic) may increase protein catabolism and plasma ammonia concentrations, thereby increasing the doses of Urea Cycle Disorder Agents needed to maintain these concentrations in the target range. Risk C: Monitor therapy
Vaccines (Inactivated/Non-Replicating): Corticosteroids (Systemic) may diminish the therapeutic effect of Vaccines (Inactivated/Non-Replicating). Management: Administer vaccines at least 2 weeks prior to immunosuppressive corticosteroids if possible. If patients are vaccinated less than 14 days prior to or during such therapy, repeat vaccination at least 3 months after therapy if immunocompetence restored. Risk D: Consider therapy modification
Vaccines (Live): Corticosteroids (Systemic) may enhance the adverse/toxic effect of Vaccines (Live). Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Vaccines (Live). Management: Avoid live vaccines during and for 1 month after therapy with immunosuppressive doses of corticosteroids (equivalent to prednisone > 2 mg/kg or 20 mg/day in persons over 10 kg for at least 2 weeks). Give live vaccines prior to therapy whenever possible. Risk D: Consider therapy modification
Vitamin K Antagonists (eg, warfarin): Corticosteroids (Systemic) may enhance the anticoagulant effect of Vitamin K Antagonists. Risk C: Monitor therapy
Yellow Fever Vaccine: Corticosteroids (Systemic) may enhance the adverse/toxic effect of Yellow Fever Vaccine. Specifically, the risk of vaccine-associated infection may be increased. Corticosteroids (Systemic) may diminish the therapeutic effect of Yellow Fever Vaccine. Risk X: Avoid combination
Systemic use of mineralocorticoids/corticosteroids may require a diet with increased potassium, vitamins A, B6, C, D, folate, calcium, zinc, and phosphorus, and decreased sodium. With fludrocortisone, a decrease in dietary sodium is often not required as the increased retention of sodium is usually the desired therapeutic effect.
Animal reproduction studies have not been conducted with fludrocortisone; adverse events have been observed with corticosteroids in animal reproduction studies. Some studies have shown an association between first trimester systemic corticosteroid use and oral clefts (Park-Wyllie 2000; Pradat 2003). Systemic corticosteroids may also influence fetal growth (decreased birth weight); however, information is conflicting (Lunghi 2010). Hypoadrenalism may occur in newborns following maternal use of corticosteroids in pregnancy; monitor.
When systemic corticosteroids are needed in pregnancy, it is generally recommended to use the lowest effective dose for the shortest duration of time, avoiding high doses during the first trimester (Leachman 2006; Lunghi 2010). Fludrocortisone may be used to treat women during pregnancy who require therapy for congenital adrenal hyperplasia or primary adrenal insufficiency (Endocrine Society [Bornstein 2016; Speiser 2018]).
Monitor blood pressure and signs of edema when patient is on chronic therapy; monitor serum electrolytes (eg, potassium, sodium, calcium), glucose, plasma renin activity. Monitor intraocular pressure (if therapy >6 weeks), linear growth of pediatric patients (with chronic use), assess HPA suppression; monitor for evidence of infection
Very potent mineralocorticoid with high glucocorticoid activity; used primarily for its mineralocorticoid effects. Promotes increased reabsorption of sodium and loss of potassium from renal distal tubules.
Metabolism: Hepatic
Half-life elimination: Plasma: ≥3.5 hours; Biological: 18 to 36 hours
In patients with salt-losing forms of congenital adrenogenital syndrome, use along with cortisone or hydrocortisone; fludrocortisone 0.1 mg has sodium retention activity equal to DOCA 1 mg
Tablets (Fludrocortisone Acetate Oral)
0.1 mg (per each): $0.75 - $0.79
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